Page 1: Introduction to Microbiology

Microbiology Overview

• Title: Microbiology with Diseases by Body System

• Chapter: 23

• Author: Robert W. Bauman

• Edition: Third Edition (2012)

• Lecture Prepared By: Mindy Miller-Kittrell, North Carolina State University

Page 2: Anatomy Review of the Digestive System

Gastrointestinal Tract

• Pathway: Extensions from mouth to anus.

• Accessory Digestive Organs: Involved in mechanical digestion and providing digestive secretions.

Functions

• Digests food

• Absorbs nutrients & water into the blood

• Eliminates waste

Page 3: Tooth Anatomy

Detailed Structure of Teeth

Components

• Bacteria: Involved in oral health.

• Gingiva (gum): Protects the underlying bones and teeth.

• Bone: Supports teeth.

• Branches of Blood Vessels and Nerve: Vital for tooth health (in root canal).

• Pulp: Soft tissue inside the tooth.

• Dentin: Adds strength.

• Enamel: Protects teeth from decay.

Page 4: Microbiota Review

Microorganisms in the Oral Cavity

• Tongue and Teeth: Host various bacteria.

• Viridans Streptococci: Most prevalent in the oral region.

Digestive Tract Regions

• Esophagus, Stomach, Duodenum: Generally microbe-free due to rapid transport and peristalsis.

• Lower Small Intestine and Colon: Rich in microbial antagonists; protected by mucous membranes.

Page 5: Dental Diseases

Dental Caries, Gingivitis, and Periodontal Disease

Signs and Symptoms

• Dental Caries: Present as holes or pits in teeth.

• Gingivitis: Gums appear swollen, tender, bright red, or bleeding.

Pathogen, Virulence, and Pathogenesis

• Streptococcus Mutans: Common cause of dental caries; uses dextran and pili for biofilm formation.

• Porphyromonas Gingivalis: Causes periodontal disease; proteases degrade gingival tissue.

Epidemiology

• High prevalence of dental caries in adults; high sucrose diets increase risk.

Diagnosis and Treatment

• Caries: Diagnosed visually; treated by fillings if early.

• Gingivitis: Diagnosed through gum inspection; treated with scaling and antibacterial rinses.

• Prevention: Good oral hygiene practices.

Page 6: Tooth Decay Process

Mechanism of Tooth Decay

• Role of Acids and Strep. Mutans:

  • Plaque (biofilm) formation leads to demineralization caused by acids.

• Involvement of Acid: Strep. mutans neutralizes acids but not completely.

Page 7: Peptic Ulcers

Signs and Symptoms

• Main Symptom: Abdominal pain.

Pathogen and Virulence

• Helicobacter Pylori: Major causative agent.

  • Virulence Factors:

    • Flagella (burrowing)

    • Adhesins (attachment)

    • Urease (neutralizes acid)

    • Toxins (damage mucosa)

Epidemiology

• Transmission: Fecal-oral.

• Stress: May exacerbate symptoms.

Diagnosis, Treatment, and Prevention

• Diagnosis: X-ray exams and clinical specimens.

• Treatment: Antimicrobials and acid inhibitors.

• Prevention: Avoid fecal-oral transmission.

Page 8: Helicobacter Pylori and Ulcers

Role of Helicobacter Pylori

• Bacteria's Impact: Invades mucus and attaches to gastric epithelial cells.

• Mechanism of Damage: Toxins and inflammation weaken the mucus layer, allowing gastric acid to damage tissues.

Page 9: Helicobacter Pylori - Formation of Ulcers

Detailed Mechanism

• Acidic Environment: Helicobacter pylori interacts with stomach acid and gastric cells, leading to ulcer formation.

Page 10: Bacterial Gastroenteritis

Overview

• Definition: Inflammation of the stomach or intestines caused by bacteria.

• Causes: Commonly linked to contaminated food or water.

Symptoms

• General symptoms include nausea, vomiting, diarrhea, abdominal pain, and cramps.

• Dysentery: Characterized by loose, frequent stools containing mucus and blood.

Page 11: Cholera as a Bacterial Gastroenteritis

Pathogenesis

• Pathogen: Vibrio cholerae.

• Virulence Factor: Cholera toxin which binds to small intestinal cells.

Epidemiology

• Historical pandemics linked to cholera outbreaks.

Diagnosis

• Observance of "rice-water stool" as a key diagnostic sign.

Treatment and Prevention

• Treatment: Supportive care and tetracycline.

• Vaccine: Available but provides short-lived immunity.

• Importance of Hygiene: Essential preventive measure.

Page 12: Impact of Dehydration Due to Cholera

Before and After Rehydration

• Visual Representation: Contrast between hydration states associated with cholera.

Page 13: Campylobacter Diarrhea

Overview

• Pathogen: Campylobacter jejuni.

• Virulence Factors: Adhesins, cytotoxins, and endotoxin.

Epidemiology

• Most common cause of diarrhea leading to doctor visits in the U.S.

Diagnosis and Treatment

• Diagnosis based on clinical symptoms; usually resolves without treatment.

• Prevention: Proper hygiene, especially after handling raw poultry.

Page 14: Campylobacter jejuni

Microscopic Appearance

• Studied Using: Transmission Electron Microscopy (TEM).

• Size: Approximately 0.3 μm in diameter.

Page 15: Antimicrobial Associated Diarrhea

Introduction

• Characterization: May result in pseudomembranous colitis in severe cases.

Pathogen and Virulence

• Causative Agent: Clostridium difficile.

  • Contributes to inflammation via toxins; resistant to multiple antibiotics.

Pathogenesis and Epidemiology

• Endospore germination is facilitated by antimicrobial use; can become life-threatening.

• Reclassification: C.difficile is now Clostridioides difficile.

Page 16: Diagnosis, Treatment, and Prevention

Detecting Infection

• Diagnosis based on bacterial toxin presence in stool.

• Treatment: Treatment with antimicrobials; avoid unnecessary prescriptions.

Page 17: Salmonellosis and Typhoid Fever

Overview

• Normal Microbiota: Salmonella species present in most vertebrates.

Pathogen and Virulence

• Causative Agents: Salmonella enterica serotypes.

  • Tolerate stomach acidity, passing into intestines.

Pathogenesis and Epidemiology

• Typhoid Fever: Acquired through contaminated food/water.

• Salmonellosis: Often from consuming contaminated eggs.

Page 18: Diagnosis and Treatment for Salmonellosis

Clinical Approach

• Diagnosis: Finding Salmonella in stool.

• Course: Salmonellosis is typically self-limiting.

• Severe Typhoid Fever: May require antimicrobial treatment; proper hygiene is crucial for prevention.

Page 19: Bacterial Food Poisoning

Overview

• Signs and Symptoms: Nausea, vomiting, diarrhea, and cramping.

Pathogen and Virulence

• Causative Agent: Staphylococcus aureus with five enterotoxins.

Pathogenesis and Epidemiology

• Common in social settings (picnics); symptoms arise within four hours of toxin ingestion.

Treatment and Prevention

• Diagnosis: Based on symptoms.

• Treatment: Focus on fluid and electrolyte replacement.

• Prevention: Emphasize proper hygiene to reduce outbreak incidence.

Page 20: Mumps

Symptoms

• Painful swelling of salivary glands, especially the parotid gland.

• Caused by the mumps virus; humans are the only natural host.

Epidemiology

• Once common in children, now rare in developed areas due to vaccination.

• Infected individuals typically develop lifelong immunity.

Page 21: Salivary Glands

Types of Salivary Glands

• Parotid Gland: Major gland affected during mumps.

• Submandibular Gland: Also contributes to saliva production.

• Sublingual Gland: Smaller gland producing saliva as well.

Page 22: Viral Gastroenteritis

Overview

• Symptoms: Comparable to bacterial gastroenteritis.

Pathogens

• Causative Agents: Caliciviruses, astroviruses, and rotaviruses.

Epidemiology

• Increased incidence in winter months.

Diagnosis, Treatment, and Prevention

• Diagnosed via serological tests; treatment relies on fluid and electrolyte balance.

• Rotavirus Impact: Major cause of infant mortality due to diarrhea; vaccines are available.

Page 23: Mortality from Rotaviral Diarrhea

Global Impact

• Significant deaths from diarrhea related to rotavirus, particularly prevalent in developing nations.

Page 24: Viral Hepatitis

Signs and Symptoms

• Includes jaundice, abdominal pain, fatigue, vomiting, and appetite loss.

• Symptoms can manifest years after initial infection.

Pathogens

• Causative Agents: HAV, HBV, HCV, HDV, and HEV.

Diagnosis, Treatment, and Prevention

• Diagnosis: Based on jaundice and serological testing for antigens.

• Recovery: Complete in 99% of HAV cases.

• Prevention: Good hygiene, safe sexual practices, vaccines for HAV and HBV.

Page 25: Comparison of Hepatitis Viruses

Implications of Infection

• Newborns at higher risk for chronic hepatitis B infections.

• Co-infection with HBV and HDV leads to severe liver damage.

Page 26: Repetitive Questions and Statements

Inquiry Focus

• Series of questions covering aspects of disease, prevention, and epidemiology, indicating a need for reflective understanding and exploration.